@Article{biocell.2026.081478,
AUTHOR = {Carmen Rubio, Norma Serrano-García, Ángel Lee, Javier Pérez-Villavicencio, Omar Villa-Robledo, Rodrigo Mercado Pimentel, Héctor Romo-Parra, Moisés Rubio-Osornio},
TITLE = {The Intersection of Impaired Ion Channels and Depleted Mitochondria in Epileptic Seizures: A Narrative Review},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27399},
ISSN = {1667-5746},
ABSTRACT = {Epilepsy is sustained by a self-reinforcing triad of ion channel dysfunction, mitochondrial impairment, and oxidative stress that lowers seizure threshold and drives epileptogenesis. This review examines how genetic channelopathies and redox-dependent post-translational modifications of voltage-gated sodium, calcium, and potassium channels disrupt excitatory–inhibitory balance, and how electron transport chain dysfunction amplifies reactive oxygen species, compromises adenosine triphosphate (ATP)-dependent membrane stability, and activates mechanistic target of rapamycin complex 1. Key convergences include oxidative ion channel modification, ATP-sensitive potassium channel impairment, synaptic lipid peroxidation, and gamma-aminobutyric acid (GABA)-ergic transporter dysfunction. Temporal lobe epilepsy is characterized by focal mitochondrial pathology, whereas genetic generalized epilepsies reflect thalamocortical channelopathies, a distinction with direct therapeutic implications. Precision strategies integrating mitochondria-targeted antioxidants, ion channel modulators, antioxidant supplementation N-acetylcysteine, α-lipoic acid, and mTOR inhibitors (rapamycin, everolimus) provide a mechanistic framework for interrupting the redox–metabolic–electrical feedback loop sustaining seizures and advancing disease modification.},
DOI = {10.32604/biocell.2026.081478}
}